MHC class II compatibility in aborted fetuses and term infants of couples with recurrent spontaneous abortion

Ober, Carole; Steck, Theodore L.; Ven, Katrin van der; Billstrand, Christine; Messer, L. A.; Kwak, Joanne Y.H.; Beaman, Kenneth D.; Beer, Alan E.

doi:10.1016/0165-0378(93)90063-n

Cited by 46 publications

(33 citation statements)

References 13 publications

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“…Ober et al [16] support such a conclusion by suggesting that HLA-DQA1-compatible fetuses may be aborted very early in pregnancy. Takakuwa et al, who were initially skeptical [17], more recently concluded [18 ]that compatibility of HLA class II antigens between husband and wife may be involved in the genesis of unexplained recurrent pregnancy loss.…”

Section: Discussionsupporting

confidence: 50%

Gestational Dermatosis Shortly after Implantation Associated with Parental Class II HLA Compatibility and Maternal Immune Activation: Preliminary Report of a Prospective Case Series

Gleicher

Barad²

2011

Dermatology

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Background: Pregnancy represents a semiallograft, subject to similar immune responses as allogeneic organ transplants. Tolerance of pregnancy appears best with maximal class II HLA heterogeneity between mother and father, while compatibilities are associated with increased pregnancy loss and maternal autoimmunity. Tolerance abnormalities often involve skin reactions. Abnormalities in tolerance of the fetal graft may do the same. Objective: To define the characteristics of a newly described dermatosis in very early pregnancy. Methods: Prospective case series of 7 couples/12 clinical episodes. Results: The dermatosis was observed in 7 out of 285 women undergoing in vitro fertilization (IVF; 2.5%; 95% CI 0.66–4.26%) and in 12 out of 277 total IVF cycles reaching embryo transfer (4.3%; 95% CI 1.93–6.73%). Prior to IVF all women reported autoimmune clinically significant allergies. All but 1 couple demonstrated class II HLA compatibility. Two of 4 pregnancies miscarried. All rashes erupted within days from embryo implantation. Conclusions: The ‘implantation rash’ reported here is uncommon but not rare. It may be the consequence of abnormal maternal immune responses to embryo implantation in women with prior immune activation, associated with class II HLA compatibility between parents. Further prospective studies are required to better define this condition.

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Section: Discussionsupporting

confidence: 50%

Gestational Dermatosis Shortly after Implantation Associated with Parental Class II HLA Compatibility and Maternal Immune Activation: Preliminary Report of a Prospective Case Series

Gleicher

Barad²

2011

Dermatology

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“…Though these latter two studies cast doubt on sharing of HLA DQ alpha 2 antigens as a cause of recurrent miscarriage, one interpretation of the first study by Ober et al is that sharing of HLA DQ alpha could lead to such early losses that it would manifest more as reduced fecundity rather than higher miscarriage rates [21]. One subsequent study, however, failed to find any association of maternal/paternal sharing of DQ alpha type II HLA antigens to be associated with pregnancy rates or miscarriage rates following IVF-ET [24].…”

Section: Discussionmentioning

confidence: 99%

“…A priori, one would think that the more allogeneic the stimulus, the more difficult it may be to suppress a maternal immune response against the fetal semi-allograft. However, there was a study published suggesting that there was a survival advantage of the fetus if it was more immunologically distinct from the mother [21]. This was based upon the demonstration that whereas 18 % of couples with recurrent miscarriage showed two similar human leukocyte antigen (HLA) DQ alpha locus alleles, this sharing was only found in only 3 % of fertile couples [21].…”

Section: Discussionmentioning

confidence: 99%

“…However, there was a study published suggesting that there was a survival advantage of the fetus if it was more immunologically distinct from the mother [21]. This was based upon the demonstration that whereas 18 % of couples with recurrent miscarriage showed two similar human leukocyte antigen (HLA) DQ alpha locus alleles, this sharing was only found in only 3 % of fertile couples [21]. This aforementioned study by Ober et al, concerning recurrent miscarriage, was not confirmed by two other studies [22,23].…”

Section: Discussionmentioning

confidence: 99%

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Evidence that exposure to progesterone alone is a sufficient stimulus to cause a precipitous rise in the immunomodulatory protein the progesterone induced blocking factor (PIBF)

Cohen

Check

Dougherty

2015

J Assist Reprod Genet

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Purpose To determine if exposure to progesterone alone is sufficient to increase the production of the immunomodulatory protein known as the progesterone induced blocking factor (PIBF). Also to determine what method of progesterone delivery or form of P best stimulates PIBF secretion. Methods Serum samples from patients with infertility and paid volunteers were evaluated for both PIBF and progesterone at various times during the follicular phase and the luteal phase in both natural cycles and cycles involving embryo transfer after endogenous and exogenous progesterone exposure and after various synthetic progestins. PIBF was measured by a non-commercial research ELISA assay. Comparisons were made of serum PIBF before and after exposure to progesterone, 17-hydroxyprogesterone, and oral contraceptives. PIBF was also measured before and after transfer of embryos.Results Progesterone alone without exposure to the fetal allogeneic stimulus was able to produce a marked increase in s e r u m P I B F. N e i t h e r a s y n t h e t i c p r o g e s t i n (19-nortestosterone derivative) nor 17-hydroxyprogesterone caused an increase in PIBF. Some PIBF is generally detected even in the follicular phase. Conclusions A previous concept considered that an allogeneic stimulus, e.g., from the fetal semi-allograft, was necessary to induce de novo progesterone receptors in gamma delta T cells, which, in turn, when exposed to a high concentration of progesterone, would secrete high levels of PIBF. These data show that exposure to an allogeneic stimulus is not needed to cause a marked rise in PIBF, merely progesterone alone is sufficient.

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“…This occurs as a result of regulation of HLA genes and complement regulatory proteins in placentas, and the establishment of an immunosuppressive environment in the pregnant uterus. Low levels of blocking antibodies have been statistically associated with maternal-paternal HLA similarity (especially with B, DP, and DQ) and with miscarriage (16,17), although this association has been challenged ( 1 8, 19). …”

Section: Paternal Leukocyte Immunizationmentioning

confidence: 99%

Clinical rheumatologic applications of reproductive immunology. Facts, fiction, and fancy

Wallace

Druzin

Lahita

1997

Arthritis & Rheumatism

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MHC class II compatibility in aborted fetuses and term infants of couples with recurrent spontaneous abortion

Cited by 46 publications

References 13 publications

Gestational Dermatosis Shortly after Implantation Associated with Parental Class II HLA Compatibility and Maternal Immune Activation: Preliminary Report of a Prospective Case Series

Gestational Dermatosis Shortly after Implantation Associated with Parental Class II HLA Compatibility and Maternal Immune Activation: Preliminary Report of a Prospective Case Series

Evidence that exposure to progesterone alone is a sufficient stimulus to cause a precipitous rise in the immunomodulatory protein the progesterone induced blocking factor (PIBF)

Clinical rheumatologic applications of reproductive immunology. Facts, fiction, and fancy

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